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Metabolism > 6. Lipid Metabolism > Flashcards

6. Lipid Metabolism Flashcards

1
Q

Structure of saturated fatty acids

A

completely saturated with hydrogen.
No double bonds.
Completely straight.
Solids

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2
Q

Structure of unsaturated fatty acids

A

Double bond inhibits rotation around the bond
= kink in chain.
Liquids

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3
Q

How are fatty acids often stored in cells?

A

As Triacylglycerols (triglycerides).

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4
Q

What cells are specialised for fatty acid storage?

A

Adipocytes

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5
Q

When are fatty acids in adipocytes used to provide energy?

A

In times of starvation

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6
Q

3 Primary sources of fat

A

Diet
De novo biosynthesis (liver)
Storage depots in adipocytes

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7
Q

What are triacylglyceriols hydrolysed to form?

A

Free fatty acids

Glycerol

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8
Q

What is a good carrier of free fatty acids?

A

Albumin

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9
Q

Where are bile salts generated and stored?

A

Generated in Liver

Stored in Gallbladder

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10
Q

Where do bile salts pass during digestion and what do they do?

A

From bile duct into intestine

Emulsify fats in intestine, aiding digestion and absorption of fats and fat-soluble vitamins (A, D, E, K)

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11
Q

What do bile salts have and what happens when they form micelles?

A

Hydrophobic face and a hydrophilic face.
When they form micelles, their hydrophilic faces face away from triacylglycerols (TAGs) and their hydrophobic faces point towards TAGs.

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12
Q

What does a lack of bile salts result in?

A

Passage of fat through the gut undigested and unabsorbed causing steatorrhea (fatty stool).

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13
Q

What is a mixed micelle?

A

A mixture of triacyl-, diacyl-, monoacylglycerols and free fatty acids with Bile Salts, Cholesterol, Lysophosphatidic Acid and fat soluble vitamins

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14
Q

What does digestion of lipids by lipase form?

A

Monoacylglycerols (MAG), diacylglycerols (DAG) and free fatty acids (FAs)

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15
Q

Where are mixed micelles absorbed and what happens?

A

By enterocytes in small intestine
Triacylglycerol reformed
Modified into chylomicrons
Enter lymphatic system

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16
Q

Orlistat

A

Lipase inhibitor
Reduces fat absorption by 30% which is excreted via faecal route
Treats obesity

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17
Q

What are the side effects of orlistat?

A

Abdominal pain
Urgency to defecate
Steatorrhea

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18
Q

Where does >50% of the body’s energy needs (except brain) come from?

A

Oxidation of fatty acids

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19
Q

Caloric yield of fatty acids relative to carbohydrates

A

Fatty acids caloric yield 2X that of carbohydrates

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20
Q

Where does Beta- Oxidation occur?

A

Mitochondria

21
Q

What does Beta-Oxidation result in formation of?

A

Acetyl CoA

22
Q

Describe beta oxidation

A

Fatty acid to acyl coA: Using 2 ATPs in outer mitochondrial membrane
Enter mitochondria by carnitine shuttle
Fatty acyl coA: oxidised and gives off FADH2
Molecule produced hydrolysed
This is then Oxidised and gives off NADH
Acetyl coA is produced by adding CoA using B KETOTHIOLASE

23
Q

What happens to the remaining fatty acyl CoA that has been shortened by 2C at the end of the Beta oxidation cycle?

A

It repeats the cycle

24
Q

What are the products of the Beta oxidation cycle?

A

1 molecule of acetyl CoA

1 acyl CoA species which is 2 carbons shorter than the original.

25
Q

Carnitine shuttle

A

Transports Acyl CoA into mitochondrial matrix by coupling it with carnitine to form Acyl carnitine

26
Q

How are carnitine and acyl carnitine moved to and from the mitochondrial matrix?

A

By a translocase

27
Q

Overall equation for breakdown of palmitate

A

Palmitoyl coA + 7FAD + 7 NAD+ + 7H20 + 7CoA
——>
8 acetyl coA + 7 FADH2 + 7 NADH

28
Q

When can acetyl coA from beta oxidation enter TCA?

A

When beta oxidation and carbohydrate metabolism are balanced as oxaloacetate is needed

29
Q

What happens if fat breakdown predominates (when fasting/ starving)?

A

Acetyl CoA forms ketone bodies e.g.
Acetoacetate
D-3-hydroxybutyrate
Acetone

30
Q

Which 2 enzymes are involved in biosynthesis of lipids?

A

Acetyl CoA carboxylase

Fatty acid synthase (FAS)

31
Q

How often and how are fatty acids formed?

A

Sequentially by decarboxylative condensation reactions involving Acetyl-CoA and Malonyl-CoA

32
Q

What happens to fatty acids following each round of elongation?

A

Undergoes reduction and dehydration by the sequential action of a ketoreductase (KR), dehydratase (DH), & enol reductase (ER) activity

33
Q

What is the growing fatty acyl group linked to and what does this provide?

A

An acyl carrier protein (ACP)
ACP provides a swinging arm mechanism to move the fatty acid chain from 1 domain to another, analogous to that of pyruvate dehydrogenase complex

34
Q

The process of lipogenesis is cycled a further 6 times from step 4-7 to yield

A

16C species: Palmitoyl-ACP

which is hydrolysed to give Palmitate and ACP

35
Q

Differences between fat metabolism and synthesis

A 
Synthesis = 
ACP carrier
NADP as reducing agent, 
Occurs in cytoplasm 
Metabolism = 
CoA carrier 
NAD+ and FAD as reducing agents 
Occurs in mitochondria
36
Q

Lipogenesis equation

A

Acetyl CoA + 7 malonyl CoA + 14 NADP + 14H+

Palmitate + CO2 +6H2O + 8 CoA + 14 NADP+

37
Q

Why is there 1 fewer H2O than expected in the lipogenesis equation?

A

1 H2O is used in the hydrolysis of Palmitoyl ACP to form Palmitate and ACP

38
Q

Where does elongation of the acyl group to make fatty acids longer than 16C occur?

A

In mitochondria and endoplasmic reticulum

39
Q

What does desaturation of fatty acids require the action of?

A

Fatty acyl-CoA desaturases

40
Q

Acyl-CoA Dehydrogenases are a family of enzymes

A

There are different types of enzymes for the different lengths of fatty acid chain.

41
Q

What length of fatty acid chain is Medium-chain acyl-Co enzyme A dehydrogenase used for?

A

C6-C12

42
Q

What length of fatty acid chain is Long-chain acyl-Co enzyme A dehydrogenase used for?

A

C13-C21

43
Q

What type of disease is Medium-chain acyl-coenzyme A dehydrogenase deficiency (MCADD)?

A

Autosomal recessive

44
Q

When and why is MCADD screened for?

A

Heel prick test

If undiagnosed= fatal, sudden infant death syndrome

45
Q

What should patients with MCADD do?

A

Never go without food >12 hours

Adhere to high carbohydrate diet

46
Q

What type of disease is Primary Carnitine deficiency?

A

Autosomal recessive

47
Q

When do symptoms of Primary Carnitine deficiency arise?

A

During infancy/ childhood

Include encephalopathies

48
Q

What causes Primary Carnitine deficiency?

A

Mutations in SLC22A5 gene which encodes a carnitine transporter
Results in reduced ability of cells to take up carnitine, needed for the β-oxidation of fatty acids.

49
Q

General structure of all fatty acids

A 
Hydrophobic carbon tail
Hydrophilic polar (charged) head

Metabolism (9 decks)

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